Although inflammation is essential for the body to protect itself against infection, when the process becomes overly aggressive it contributes to a host of inflammatory conditions including inflammatory bowel diseases, heart disease, autoimmune disorders, and sepsis. The laboratory studies the molecular mechanisms by which blood phagocytes such as macrophages and dendritic cells recognize microbial pathogens and initiate inflammatory responses. Further, a central question in immunology is to understand how inflammatory responses become tailored to specific microbial infections, and we hypothesize that phagocytosis, the process by which these cells eat foreign microbes, is a key part of this. The laboratory has used coordinated recognition of fungal pathogens by the C-type lectin receptor Dectin-1, and the Toll-like receptor TLR2 as a model for defining how different innate immune receptors can work together to orchestrate very specific inflammatory responses. Hopefully, understanding in exquisite detail how macrophages and dendritic cells translate recognition of microbes into inflammatory responses will lead to the design of targeted interventions to clinically manipulate these processes.
Key contributions to our understanding of how innate immunity initiates host defense. Have specifically championed the role of phagocytes in immunity and the role of phagocytosis in signal transduction.
Defining signal transduction mechanisms activated by innate immune receptors in macrophages and dendritic cells. Learning about how these signals can be modified to shape inflammatory responses - both for improved host defense and for tempering the inflammatory tissue damage that is often associated with active immunity.
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